Obesity is a metabolic disorder that can be caused by numerous factors such as diet, environment, lifestyle and genetics. In addition to weight gain, it can lead to a series of complications, including diabetes, hypertension, hyperlipidemia, and heart disease. For the in-depth study of the pathogenesis of obesity and the evaluation of relevant therapeutics, GemPharmatech has developed a series of obesity mouse models, including diet-induced obesity models, genetic mutation-induced spontaneous obesity models, chromosomal substitution-based obesity model.
An 11-bp base deletion in exon 8 of the Alms1 gene in C57BL/6JGpt mice led to early termination of translation of the Alms1 gene, leading to a combined phenotype of obesity, early diabetes and non-alcoholic fatty liver disease. These mice are ideal models for studies on obesity and fatty liver.
Chromosome Segment Substitution Lines (CSSL)
After 8 weeks of age, D000750 mice develop spontaneous obesity with significantly elevated cholesterol levels and mildly elevated blood glucose levels. These mice can develop a fatty liver phenotype with age and are applicable to studies on fatty liver disease, hyperlipidemia, cardiovascular disease, and obesity. Western diet (WD) induction accelerates the appearance of NASH symptoms.
Moderate obesity and mild insulin resistance are induced with a 60% high-fat diet in C57BL/6JGpt mice. These mice are applicable to studies on obesity and obesity-related complications.
In C57BL/6JGpt mice, knocking out the Leptin gene causes severe morbid obesity, temporary blood glucose elevation, compensatory expansion of the islets of the Langerhans, and severe insulin resistance, with mild complications.